THE MEASUREMENT OF TRIGLYCERIDE IN BRAIN AND THE METABOLISM OF BRAIN TRIGLYCERIDE <i>IN VITRO</i>

Rowe, Charles E.

doi:10.1111/j.1471-4159.1969.tb05938.x

Cited by 51 publications

(21 citation statements)

References 24 publications

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“…Those authors concluded that the increase in glycerol reflected membrane phospholipid breakdown as glycerol is an end product of membrane phospholipid hydrolysis and as other possible sources were not likely. Thus triglycerides are only found in trace amounts in brain tissue27 28 and during ischaemia carbohydrate stores are quantitatively transformed into lactate 29. Although the transport mechanisms of glycerol between the extracellular and intracellular compartments are not known, we assume that the increases of interstitial glycerol found in this study reflect the same phenomenon as in experimental brain ischaemia—that is, membrane phospholipid degradation.…”

Section: Discussionmentioning

confidence: 50%

Interstitial glycerol as a marker for membrane phospholipid degradation in the acutely injured human brain

Hillered

Valtysson

Enblad

et al. 1998

Journal of Neurology, Neurosurgery & Psychiatry

240

143

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Objective-Brain interstitial glycerol was studied as a potential marker for membrane phospholipid degradation in acute human brain injury. Methods-Glycerol was measured in microdialysis samples from the frontal lobe cortex in four patients in the neurointensive care unit, during the acute phase after severe aneurysmal subarachnoid haemorrhage. Microdialysis probes were inserted in conjunction with a ventriculostomy used for routine intracranial pressure monitoring. Clinical events involving hypoxia/ischaemia were diagnosed by neurological signs, neuroimaging (CT and PET), and neurochemical changes of the dialysate-for example, lactate/pyruvate ratios and hypoxanthine concentrations. Results-Altogether 1554 chemical analyses on 518 microdialysis samples were performed. Clinical events involving secondary hypoxia/ischaemia were generally associated with pronounced increases (up to 15-fold) of the dialysate glycerol concentration. In a patient with a stable condition and no signs of secondary hypoxia/ischaemia the glycerol concentration remained low. Simultaneous determination of glycerol in arterial plasma samples showed that the changes in brain interstitial glycerol could not be attributed to systemic changes and an injured blood brain barrier. Conclusions-This study suggests that membrane phospholipid degradation occurs in human cerebral ischaemia. Interstitial glycerol harvested by microdialysis seems to be a promising tool for monitoring of membrane lipolysis in acute brain injury. The marker may be useful for studies on cell membrane injury mechanisms mediated by for example, Ca 2+ disturbances, excitatory amino acids, and reactive oxygen species; and in the evaluation of new neuroprotective therapeutic strategies. (J Neurol Neurosurg Psychiatry 1998;64:486-491)

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Section: Discussionmentioning

confidence: 50%

Interstitial glycerol as a marker for membrane phospholipid degradation in the acutely injured human brain

Hillered

Valtysson

Enblad

et al. 1998

Journal of Neurology, Neurosurgery & Psychiatry

240

143

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“…Some of the abnormalities in lipid composition that we report in this study may contribute to this resistance. For example, the decreased brain triacylglycerol concentration in the COX-2 2/2 mouse may increase its resistance to ischemia/reperfusion damage (9,12), because triacylglycerol can be a source of nutrient fatty acids for brain phospholipid biosynthesis (35)(36)(37) and its concentration is increased in cerebral ischemia (38,39).…”

Section: Discussionmentioning

confidence: 99%

Altered brain lipid composition in cyclooxygenase-2 knockout mouse

Langenbach

Rapoport

et al. 2007

Journal of Lipid Research

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Cyclooxygenase (COX)-2 plays an important role in brain arachidonic acid (20:4n-6) metabolism, and its expression is upregulated in animal models of neuroinflammation and excitotoxicity. Our hypothesis was that brain lipid composition would be altered in COX-2 knockout (COX-2 2/2 ) compared with wild-type (COX-2 1/1 ) mice, reflecting the important role of COX-2 in brain lipid metabolism. Concentrations of different lipids were measured in high-energy microwaved brain from COX-2 2/2 and COX-2 1/1 mice. Compared with the COX-2 1/1 mouse brain, the brain of the COX-2 2/2 mouse had a statistically significant 15% increase in phosphatidylserine (PtdSer) and significant 37, 27, and 32% reductions in triacylglycerol and cholesterol concentrations and in the cholesterol-tophospholipid ratio, respectively. The normalized concentration of palmitic acid (16:0) was increased in PtdSer, as was the brain concentration of unesterified arachidic acid (20:0). A lifetime absence of COX-2 produces multiple changes in brain lipid composition. These changes may be related to reported changes in fatty acid kinetics and in resistance to neuroinflammation and excitotoxicity in the COX-2 2/2 mouse.-Ma, K., R. Langenbach, S. I. Rapoport, and M. Basselin. Altered brain lipid composition in cyclooxygenase-2 knockout mouse. J. Lipid Res. 2007. 48: 848-854.

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“…Since palmitate was elongated and desaturated by brain slices only to a slight extent, this may restrict the acylation of radioactive fatty acid into the glyceride fraction. It has been suggested that the small pool of triglyceride present in brain has a high rate of turnover of the acyl moiety (ROWE, 1969) thereby making acyl groups available for further metabolism by elongation or desaturation (MENKES, 1971). Over the time period used in this study (1-5 h) incor-poration of radioactivity into glycerides was always greater than into phospholipids.…”

Section: Discussionmentioning

confidence: 99%

“…The extent to which palmitate derived from the turnover of specific lipid types e.g. triglyceride (ROWE, 1969) or phosphatidylcholine (SUN & HORROCKS, 1971) contributes to the pool of free fatty acid (synthesized de nouo or from exogenous fatty acid) is difficult to assess. The turnover of esterified fatty acid may constitute a second pool of membrane-bound fatty acid, distinct from the pool of free fatty acids synthesized in the cell cytoplasm, which could undergo different metabolic reaction sequences to the free fatty acid in the cell cytoplasm.…”

Section: Discussionmentioning

confidence: 99%

A COMPARATIVE STUDY OF THE METABOLISM OF DE NOVO SYNTHESIZED FATTY ACIDS FROM ACETATE AND GLUCOSE, AND EXOGENOUS FATTY ACIDS, IN SLICES OF RABBIT CEREBRAL CORTEX DURING DEVELOPMENT

Carey

1975

Journal of Neurochemistry

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Abstract— Slices of rabbit cerebral cortex, from the foetal stage to the adult have been used to compare lipid synthesis from fatty acids synthesized de novo from [U‐14C]glucose and [1‐14C]acetate, with lipid synthesis from exogenous albumin‐bound [1‐14C]palmitate. Incorporation into cellular lipid has been determined in terms of DNA, protein, wet wt. of tissue and wet weight of whole brain. On a wet wt. basis, maximum incorporation of glucose carbon into lipid occurred in the foetal brain while lipid synthesis from acetate and palmitate was maximum at 4–14 days after birth. Glucose and acetate were incorporated into a diversity of lipids (with increasing amounts of phosphatidylcholine synthesized during maturation), while palmitate was incorporated into the free fatty acid and triglyceride fractions. A greater proportion of acetate was incorporated into fatty acids of chain‐length longer than C16 compared with the incorporation of palmitate. However, on a molar basis de novo synthesized and exogenous palmitate were elongated, desaturated and incorporated into phospholipids at a similar rate, while exogenous palmitate was incorporated to a greater extent than de nova synthesized fatty acid into the triglyceride fraction. This difference in metabolism may be due to the different size of the non‐esterified fatty acid pool in the two situations. At the period of their most active formation, the very long‐chain fatty acids may be synthesized from a pool of the C18 series of fatty acids (saturated and monoenoic) not in equilibrium with the bulk of C18 acids in cerebral lipids. This could be a pool of acyl groups derived from ethanolamine phospholipids.

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THE MEASUREMENT OF TRIGLYCERIDE IN BRAIN AND THE METABOLISM OF BRAIN TRIGLYCERIDE IN VITRO

Cited by 51 publications

References 24 publications

Interstitial glycerol as a marker for membrane phospholipid degradation in the acutely injured human brain

Interstitial glycerol as a marker for membrane phospholipid degradation in the acutely injured human brain

Altered brain lipid composition in cyclooxygenase-2 knockout mouse

A COMPARATIVE STUDY OF THE METABOLISM OF DE NOVO SYNTHESIZED FATTY ACIDS FROM ACETATE AND GLUCOSE, AND EXOGENOUS FATTY ACIDS, IN SLICES OF RABBIT CEREBRAL CORTEX DURING DEVELOPMENT

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